Neuronal GPT

1. Active induction via FGF (niewcoop center)

2. Permissive induction (bmp inhibitors)

Neural induction is the process by which ectodermal cells are instructed to develop into neural tissue. Mechanisms mediating neural induction include signals from the Spemann organizer, particularly the secretion of molecules like Noggin, Chordin, and Follistatin, which inhibit BMP signaling to promote neural fate.

Neurulation involves the formation of the neural tube. Initially, the neural plate thickens, folds, and forms neural folds that converge and fuse at the dorsal midline, creating the neural tube. This process includes primary neurulation (folding) and secondary neurulation (cavitation in the caudal region).

The neural anlage initially has anterior CNS characteristics, which are later "posteriorized" by signals like FGF, WNT, and retinoic acid.

The two forms of neurulation are primary neurulation, where the neural plate folds to form the neural tube, and secondary neurulation, where a solid rod of cells forms and then hollows out to become the neural tube.

Planar signals are distributed along the neural plate and influence patterning horizontally (e.g., WNT and FGF signals). Vertical signals are sent from underlying mesodermal structures (e.g., Shh from the notochord and BMP from the epidermis) to establish dorso-ventral patterning.

The Spemann Organizer induces neural tissue formation, patterns the neural axis, and secretes factors (e.g., Noggin, Chordin) that inhibit BMP signaling to specify neural ectoderm.

Shh from the notochord induces ventral characteristics, while BMPs from the roof plate specify dorsal characteristics. Gradients of these signals define the dorso-ventral axis.

Transplanting a notochord near ectopic dorsal neural tissue induces ventral cell types (e.g., motor neurons), demonstrating the notochord's role as a ventral signaling center via Shh.

WNT, FGF, and retinoic acid signaling posteriorize the neural plate by suppressing anterior fates and promoting hindbrain and spinal cord development.

WNT signals can be visualized using reporter assays with WNT-responsive promoters driving fluorescent proteins, or by immunostaining for β-catenin, a WNT signaling mediator.

Key organizing centers include the Spemann organizer, the isthmic organizer (midbrain-hindbrain boundary), and the roof and floor plates.

The transplanted isthmus induces midbrain and cerebellar structures in the diencephalon, demonstrating its role as an organizer.

It regulates regional identity, neuronal differentiation, and patterning through FGF8 and WNT signaling.

Yes, the hindbrain is segmented into rhombomeres, defined by distinct gene expression boundaries and lineage restriction.

Labeling cells with lineage tracers and observing restricted migration patterns within segments, or analyzing segment-specific gene expression (e.g., Hox genes).

Retinoic acid binds nuclear RA receptors (RAR/RXR), which act as transcription factors to regulate gene expression, particularly Hox genes.

RA is synthesized in posterior regions and degraded by enzymes like CYP26A1 in anterior regions, creating a gradient.

RA regulates Hox gene expression to specify rhombomere identity in the hindbrain.

Neurogenesis is the process by which neural progenitor cells differentiate into neurons.

Notch signaling maintains progenitor status by lateral inhibition, while reduced Notch activity in certain cells allows them to differentiate into neurons.

Notch signaling keeps some cells as progenitors, ensuring a balance between differentiation and proliferation. Non-neuronal cells can become glial cells or remain progenitors.

The brain grows through cell proliferation, the expansion of progenitor pools, neurogenesis, gliogenesis, and synaptic connections.

Yes, new neurons are formed in the hippocampus (dentate gyrus) and the subventricular zone.

Neural stem cell niches include progenitors, supporting cells (e.g., astrocytes), vasculature, and extracellular matrix, providing signals that regulate stem cell behavior.

Neuronal identity is defined by gradients of morphogens (e.g., Shh, BMP) and region-specific transcription factors that control gene expression.

1. Neural induction

2. Neurulation

3. Regional patterning

4. Neurogenesis

5. Neuronal migration

6. Axon guidance

7. Synaptogenesis

8. Circuit formation

Axons are guided by chemoattraction, chemorepulsion, contact attraction, and contact repulsion, mediated by molecules like netrins, semaphorins, slits, and ephrins.

Retinal ganglion cells project to the tectum using gradients of ephrins and Eph receptors, which ensure spatially organized connectivity, creating a retinotopic map.